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What is diabetes?

Diabetes is a complex group of diseases with a variety of causes. People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia.

Diabetes is a disorder of metabolism—the way the body uses digested food for energy. The digestive tract breaks down carbohydrates—sugars and starches found in many foods—into glucose, a form of sugar that enters the bloodstream. With the help of the hormone insulin, cells throughout the body absorb glucose and use it for energy. Diabetes develops when the body doesn’t make enough insulin or is not able to use insulin effectively, or both.

Insulin is made in the pancreas, an organ located behind the stomach. The pancreas contains clusters of cells called islets. Beta cells within the islets make insulin and release it into the blood.

Islets within the pancreas contain beta cells,
which make insulin and release it into the blood.

If beta cells don’t produce enough insulin, or the body doesn’t respond to the insulin that is present, glucose builds up in the blood instead of being absorbed by cells in the body, leading to prediabetes or diabetes. Prediabetes is a condition in which blood glucose levels or A1C levels—which reflect average blood glucose levels—are higher than normal but not high enough to be diagnosed as diabetes. In diabetes, the body’s cells are starved of energy despite high blood glucose levels.

Over time, high blood glucose damages nerves and blood vessels, leading to complications such as heart disease, stroke, kidney disease, blindness, dental disease, and amputations. Other complications of diabetes may include increased susceptibility to other diseases, loss of mobility with aging, depression, and pregnancy problems. No one is certain what starts the processes that cause diabetes, but scientists believe genes and environmental factors interact to cause diabetes in most cases.

The two main types of diabetes are type 1 diabetes and type 2 diabetes. A third type, gestational diabetes, develops only during pregnancy. Other types of diabetes are caused by defects in specific genes, diseases of the pancreas, certain drugs or chemicals, infections, and other conditions. Some people show signs of both type 1 and type 2 diabetes.

What causes type 1 diabetes?

Type 1 diabetes is caused by a lack of insulin
due to the destruction of insulin-producing
beta cells in the pancreas. In type 1
diabetes—an autoimmune disease—the
body’s immune system attacks and destroys
the beta cells. Normally, the immune system
protects the body from infection by identifying
and destroying bacteria, viruses, and
other potentially harmful foreign substances.
But in autoimmune diseases, the immune
system attacks the body’s own cells. In type 1
diabetes, beta cell destruction may take
place over several years, but symptoms of the
disease usually develop over a short period
of time.

Type 1 diabetes typically occurs in children
and young adults, though it can appear at
any age. In the past, type 1 diabetes was
called juvenile diabetes or insulin-dependent
diabetes mellitus.

Latent autoimmune diabetes in adults
(LADA) may be a slowly developing kind
of type 1 diabetes. Diagnosis usually occurs
after age 30. In LADA, as in type 1 diabetes,
the body’s immune system destroys the beta
cells. At the time of diagnosis, people with
LADA may still produce their own insulin,
but eventually most will need insulin shots
or an insulin pump to control blood glucose
levels.

Genetic Susceptibility

Heredity plays an important part in determining
who is likely to develop type 1 diabetes.
Genes are passed down from biological
parent to child. Genes carry instructions
for making proteins that are needed for the
body’s cells to function. Many genes, as well
as interactions among genes, are thought
to influence susceptibility to and protection
from type 1 diabetes. The key genes may
vary in different population groups. Variations
in genes that affect more than 1 percent
of a population group are called gene
variants.

Certain gene variants that carry instructions
for making proteins called human leukocyte
antigens (HLAs) on white blood cells are
linked to the risk of developing type 1 diabetes.
The proteins produced by HLA genes
help determine whether the immune system
recognizes a cell as part of the body or as foreign
material. Some combinations of HLA
gene variants predict that a person will be at
higher risk for type 1 diabetes, while other
combinations are protective or have no effect
on risk.

While HLA genes are the major risk genes
for type 1 diabetes, many additional risk
genes or gene regions have been found. Not
only can these genes help identify people at
risk for type 1 diabetes, but they also provide
important clues to help scientists better
understand how the disease develops and
identify potential targets for therapy and
prevention.

Genetic testing can show what types of HLA
genes a person carries and can reveal other
genes linked to diabetes. However, most
genetic testing is done in a research setting
and is not yet available to individuals. Scientists
are studying how the results of genetic
testing can be used to improve type 1 diabetes
prevention or treatment.

Autoimmune Destruction of Beta Cells

In type 1 diabetes, white blood cells called
T cells attack and destroy beta cells. The
process begins well before diabetes symptoms
appear and continues after diagnosis.
Often, type 1 diabetes is not diagnosed until
most beta cells have already been destroyed.
At this point, a person needs daily insulin
treatment to survive. Finding ways to modify
or stop this autoimmune process and preserve
beta cell function is a major focus of
current scientific research.

Recent research suggests insulin itself may
be a key trigger of the immune attack on
beta cells. The immune systems of people
who are susceptible to developing type 1
diabetes respond to insulin as if it were a
foreign substance, or antigen. To combat
antigens, the body makes proteins called
antibodies. Antibodies to insulin and other
proteins produced by beta cells are found in
people with type 1 diabetes. Researchers test
for these antibodies to help identify people
at increased risk of developing the disease.
Testing the types and levels of antibodies in
the blood can help determine whether a person
has type 1 diabetes, LADA, or another
type of diabetes.

Environmental Factors

Environmental factors, such as foods, viruses,
and toxins, may play a role in the development
of type 1 diabetes, but the exact nature
of their role has not been determined. Some
theories suggest that environmental factors
trigger the autoimmune destruction of beta
cells in people with a genetic susceptibility
to diabetes. Other theories suggest that
environmental factors play an ongoing role in
diabetes, even after diagnosis.

Viruses and infections. A virus cannot cause
diabetes on its own, but people are sometimes
diagnosed with type 1 diabetes during
or after a viral infection, suggesting a link
between the two. Also, the onset of type 1
diabetes occurs more frequently during the
winter when viral infections are more common.
Viruses possibly associated with type 1
diabetes include coxsackievirus B, cytomegalovirus,
adenovirus, rubella, and mumps. Scientists have described several ways these
viruses may damage or destroy beta cells or
possibly trigger an autoimmune response in
susceptible people. For example, anti-islet
antibodies have been found in patients with
congenital rubella syndrome, and cytomegalovirus
has been associated with significant
beta cell damage and acute pancreatitis––inflammation of the pancreas. Scientists are
trying to identify a virus that can cause type 1
diabetes so that a vaccine might be developed
to prevent the disease.

Infant feeding practices. Some studies have
suggested that dietary factors may raise or
lower the risk of developing type 1 diabetes.
For example, breastfed infants and infants
receiving vitamin D supplements may have
a reduced risk of developing type 1 diabetes,
while early exposure to cow’s milk and cereal
proteins may increase risk. More research is
needed to clarify how infant nutrition affects
the risk for type 1 diabetes.

Read more in the Centers for Disease
Control and Prevention’s (CDC’s)
publication National Diabetes Statistics
Report, 2014 at www.cdc.gov for
information about research studies
related to type 1 diabetes.

What causes type 2 diabetes?

Type 2 diabetes—the most common form
of diabetes—is caused by a combination of
factors, including insulin resistance, a condition
in which the body’s muscle, fat, and liver
cells do not use insulin effectively. Type 2
diabetes develops when the body can no
longer produce enough insulin to compensate
for the impaired ability to use insulin.
Symptoms of type 2 diabetes may develop
gradually and can be subtle; some people
with type 2 diabetes remain undiagnosed for
years.

Type 2 diabetes develops most often in
middle-aged and older people who are also
overweight or obese. The disease, once
rare in youth, is becoming more common in
overweight and obese children and adolescents.
Scientists think genetic susceptibility
and environmental factors are the most likely
triggers of type 2 diabetes.

Genetic Susceptibility

Genes play a significant part in susceptibility
to type 2 diabetes. Having certain genes
or combinations of genes may increase or
decrease a person’s risk for developing the
disease. The role of genes is suggested by
the high rate of type 2 diabetes in families
and identical twins and wide variations in
diabetes prevalence by ethnicity. Type 2
diabetes occurs more frequently in African
Americans, Alaska Natives, American
Indians, Hispanics/Latinos, and some Asian
Americans, Native Hawaiians, and Pacific
Islander Americans than it does in non-Hispanic whites.

Recent studies have combined genetic data
from large numbers of people, accelerating
the pace of gene discovery. Though scientists
have now identified many gene variants
that increase susceptibility to type 2 diabetes,
the majority have yet to be discovered. The
known genes appear to affect insulin production
rather than insulin resistance. Researchers
are working to identify additional gene
variants and to learn how they interact with
one another and with environmental factors
to cause diabetes.

Studies have shown that variants of the
TCF7L2 gene increase susceptibility to type 2
diabetes. For people who inherit two copies
of the variants, the risk of developing type 2
diabetes is about 80 percent higher than for
those who do not carry the gene variant.1
However, even in those with the variant, diet
and physical activity leading to weight loss
help delay diabetes, according to the Diabetes
Prevention Program (DPP), a major clinical
trial involving people at high risk.

Genes can also increase the risk of diabetes
by increasing a person’s tendency to become
overweight or obese. One theory, known as
the “thrifty gene” hypothesis, suggests certain
genes increase the efficiency of metabolism
to extract energy from food and store
the energy for later use. This survival trait
was advantageous for populations whose
food supplies were scarce or unpredictable
and could help keep people alive during
famine. In modern times, however, when
high-calorie foods are plentiful, such a trait
can promote obesity and type 2 diabetes.

Obesity and Physical Inactivity

Physical inactivity and obesity are strongly
associated with the development of type 2
diabetes. People who are genetically susceptible
to type 2 diabetes are more vulnerable
when these risk factors are present.

An imbalance between caloric intake and
physical activity can lead to obesity, which
causes insulin resistance and is common in
people with type 2 diabetes. Central obesity,
in which a person has excess abdominal fat,
is a major risk factor not only for insulin
resistance and type 2 diabetes but also for
heart and blood vessel disease, also called
cardiovascular disease (CVD). This excess
“belly fat” produces hormones and other
substances that can cause harmful, chronic
effects in the body such as damage to blood
vessels.

The DPP and other studies show that millions
of people can lower their risk for type 2
diabetes by making lifestyle changes and
losing weight. The DPP proved that people
with prediabetes—at high risk of developing
type 2 diabetes—could sharply lower
their risk by losing weight through regular
physical activity and a diet low in fat and
calories. In 2009, a follow-up study of DPP
participants—the Diabetes Prevention Program
Outcomes Study (DPPOS)—showed
that the benefits of weight loss lasted for at
least 10 years after the original study began.2

Read more about the DPP, funded under
National Institutes of Health (NIH)
clinical trial number NCT00004992, and
the DPPOS, funded under NIH clinical
trial number NCT00038727 in Diabetes
Prevention Program at www.diabetes.niddk.nih.gov.

Insulin Resistance

Insulin resistance is a common condition in
people who are overweight or obese, have
excess abdominal fat, and are not physically
active. Muscle, fat, and liver cells stop
responding properly to insulin, forcing the
pancreas to compensate by producing extra
insulin. As long as beta cells are able to
produce enough insulin, blood glucose levels
stay in the normal range. But when insulin
production falters because of beta cell
dysfunction, glucose levels rise, leading to
prediabetes or diabetes.

Abnormal Glucose Production by the Liver

In some people with diabetes, an abnormal
increase in glucose production by the liver
also contributes to high blood glucose levels.
Normally, the pancreas releases the hormone
glucagon when blood glucose and insulin
levels are low. Glucagon stimulates the liver
to produce glucose and release it into the
bloodstream. But when blood glucose and
insulin levels are high after a meal, glucagon
levels drop, and the liver stores excess
glucose for later, when it is needed. For
reasons not completely understood, in many
people with diabetes, glucagon levels stay
higher than needed. High glucagon levels
cause the liver to produce unneeded glucose,
which contributes to high blood glucose
levels. Metformin, the most commonly used
drug to treat type 2 diabetes, reduces glucose
production by the liver.

The Roles of Insulin and Glucagon in Normal Blood Glucose
Regulation

A healthy person’s body keeps blood glucose levels in a normal range through several complex
mechanisms. Insulin and glucagon, two hormones made in the pancreas, help regulate
blood glucose levels:

Insulin, made by beta cells, lowers elevated blood glucose levels.

Glucagon, made by alpha cells, raises low blood glucose levels.

When blood glucose levels rise after a meal,
the pancreas releases insulin into the blood.

Insulin stimulates the liver and muscle
tissue to store excess glucose. The stored
form of glucose is called glycogen.

Insulin also lowers blood glucose levels by
reducing glucose production in the liver.

When blood glucose levels drop overnight or
due to a skipped meal or heavy exercise, the
pancreas releases glucagon into the blood.

Glucagon signals the liver and muscle tissue
to break down glycogen into glucose,
which enters the bloodstream and raises
blood glucose levels.

If the body needs more glucose, glucagon
stimulates the liver to make glucose from
amino acids.

Insulin and glucagon help regulate blood
glucose
levels.

Metabolic Syndrome

Metabolic syndrome, also called insulin
resistance syndrome, refers to a group of
conditions common in people with insulin
resistance, including

higher than normal blood glucose levels

increased waist size due to excess
abdominal fat

high blood pressure

abnormal levels of cholesterol and triglycerides
in the blood

People with metabolic syndrome have an
increased risk of developing type 2 diabetes
and CVD. Many studies have found that
lifestyle changes, such as being physically
active and losing excess weight, are the best
ways to reverse metabolic syndrome, improve
the body’s response to insulin, and reduce
risk for type 2 diabetes and CVD.

Cell Signaling and Regulation

Cells communicate through a complex network
of molecular signaling pathways. For
example, on cell surfaces, insulin receptor
molecules capture, or bind, insulin molecules
circulating in the bloodstream. This
interaction between insulin and its receptor
prompts the biochemical signals that enable
the cells to absorb glucose from the blood
and use it for energy.

Problems in cell signaling systems can set
off a chain reaction that leads to diabetes or
other diseases. Many studies have focused
on how insulin signals cells to communicate
and regulate action. Researchers
have identified proteins and pathways
that transmit the insulin signal and have
mapped interactions between insulin and
body tissues, including the way insulin
helps the liver control blood glucose levels.
Researchers have also found that key signals
also come from fat cells, which produce substances
that cause inflammation and insulin
resistance.

This work holds the key to combating
insulin resistance and diabetes. As scientists
learn more about cell signaling systems
involved in glucose regulation, they will
have more opportunities to develop effective
treatments.

Scientists have not determined the causes of
beta cell dysfunction in most cases. Single
gene defects lead to specific forms of diabetes
called maturity-onset diabetes of
the young (MODY). The genes involved
regulate insulin production in the beta
cells. Although these forms of diabetes are
rare, they provide clues as to how beta cell
function may be affected by key regulatory
factors. Other gene variants are involved in
determining the number and function of beta
cells. But these variants account for only a
small percentage of type 2 diabetes cases.
Malnutrition early in life is also being investigated
as a cause of beta cell dysfunction.
The metabolic environment of the developing
fetus may also create a predisposition for
diabetes later in life.

Risk Factors for Type 2 Diabetes

People who develop type 2 diabetes
are more likely to have the following
characteristics:

age 45 or older

overweight or obese

physically inactive

parent or sibling with diabetes

family background that is African
American, Alaska Native, American
Indian, Asian American, Hispanic/Latino, or Pacific Islander American

history of giving birth to a baby
weighing more than 9 pounds

history of gestational diabetes

high blood pressure—140/90 or
above—or being treated for high
blood pressure

prediabetes—an A1C level of 5.7 to
6.4 percent; a fasting plasma glucose
test result of 100–125 mg/dL, called
impaired fasting glucose; or a 2-hour
oral glucose tolerance test result of
140–199, called impaired glucose
tolerance

acanthosis nigricans, a condition associated
with insulin resistance, characterized
by a dark, velvety rash around
the neck or armpits

history of CVD

The American Diabetes Association (ADA)
recommends that testing to detect prediabetes
and type 2 diabetes be considered
in adults who are overweight or obese and
have one or more additional risk factors for
diabetes. In adults without these risk factors,
testing should begin at age 45.

What causes gestational diabetes?

Scientists believe gestational diabetes is
caused by the hormonal changes and metabolic
demands of pregnancy together with
genetic and environmental factors.

Insulin Resistance and Beta Cell Dysfunction

Hormones produced by the placenta and
other pregnancy-related factors contribute to
insulin resistance, which occurs in all women
during late pregnancy. Insulin resistance
increases the amount of insulin needed to
control blood glucose levels. If the pancreas
can’t produce enough insulin due to beta cell
dysfunction, gestational diabetes occurs.

As with type 2 diabetes, excess weight is
linked to gestational diabetes. Overweight
or obese women are at particularly high risk
for gestational diabetes because they start
pregnancy with a higher need for insulin due
to insulin resistance. Excessive weight gain
during pregnancy may also increase risk.

Family History

Having a family history of diabetes is also
a risk factor for gestational diabetes, suggesting
that genes play a role in its development.
Genetics may also explain why
the disorder occurs more frequently in
African Americans, American Indians, and
Hispanics/Latinos. Many gene variants
or combinations of variants may increase
a woman’s risk for developing gestational
diabetes. Studies have found several gene
variants associated with gestational diabetes,
but these variants account for only a small
fraction of women with gestational diabetes.

Future Risk of Type 2 Diabetes

Because a woman’s hormones usually return
to normal levels soon after giving birth, gestational
diabetes disappears in most women
after delivery. However, women who have gestational diabetes are more likely to develop gestational diabetes with future pregnancies and develop type 2 diabetes.3 Women
with gestational diabetes should be tested for
persistent diabetes 6 to 12 weeks after delivery
and at least every 3 years thereafter.

Also, exposure to high glucose levels during
gestation increases a child’s risk for becoming
overweight or obese and for developing
type 2 diabetes later on. The result may be
a cycle of diabetes affecting multiple generations
in a family. For both mother and child,
maintaining a healthy body weight and being
physically active may help prevent type 2
diabetes.

Other Types and Causes of Diabetes

Other types of diabetes have a variety of possible
causes.

Genetic Mutations Affecting Beta
Cells, Insulin, and Insulin Action

Some relatively uncommon forms of diabetes
known as monogenic diabetes are caused
by mutations, or changes, in a single gene.
These mutations are usually inherited, but
sometimes the gene mutation occurs spontaneously.
Most of these gene mutations cause
diabetes by reducing beta cells’ ability to
produce insulin.

The most common types of monogenic diabetes
are neonatal diabetes mellitus (NDM) and
MODY. NDM occurs in the first 6 months
of life. MODY is usually found during adolescence
or early adulthood but sometimes
is not diagnosed until later in life. For more
information about NDM and MODY, see the
NDIC fact sheet Monogenic Forms of Diabetes at www.diabetes.niddk.nih.gov.

Other rare genetic mutations can cause diabetes
by damaging the quality of insulin the
body produces or by causing abnormalities in
insulin receptors.

Other Genetic Diseases

Diabetes occurs in people with Down syndrome,
Klinefelter syndrome, and Turner
syndrome at higher rates than the general
population. Scientists are investigating
whether genes that may predispose people to
genetic syndromes also predispose them to
diabetes.

The genetic disorders cystic fibrosis and
hemochromatosis are linked to diabetes.
Cystic fibrosis produces abnormally thick
mucus, which blocks the pancreas. The risk
of diabetes increases with age in people with
cystic fibrosis. Hemochromatosis causes the
body to store too much iron. If the disorder
is not treated, iron can build up in and damage
the pancreas and other organs.

Damage to or Removal of the Pancreas

Pancreatitis, cancer, and trauma can all harm
the pancreatic beta cells or impair insulin
production, thus causing diabetes. If the
damaged pancreas is removed, diabetes will
occur due to the loss of the beta cells.

Endocrine Diseases

Endocrine diseases affect organs that produce
hormones. Cushing’s syndrome and
acromegaly are examples of hormonal disorders
that can cause prediabetes and diabetes
by inducing insulin resistance. Cushing’s
syndrome is marked by excessive production
of cortisol—sometimes called the “stress hormone.”
Acromegaly occurs when the body
produces too much growth hormone. Glucagonoma,
a rare tumor of the pancreas, can
also cause diabetes. The tumor causes the
body to produce too much glucagon. Hyperthyroidism,
a disorder that occurs when the
thyroid gland produces too much thyroid
hormone, can also cause elevated blood
glucose levels.

Autoimmune Disorders

Rare disorders characterized by antibodies
that disrupt insulin action can lead to diabetes.
This kind of diabetes is often associated
with other autoimmune disorders such as
lupus erythematosus. Another rare autoimmune
disorder called stiff-man syndrome is
associated with antibodies that attack the
beta cells, similar to type 1 diabetes.

Medications and Chemical Toxins

Some medications, such as nicotinic acid
and certain types of diuretics, anti-seizure
drugs, psychiatric drugs, and drugs to treat
human immunodeficiency virus (HIV), can
impair beta cells or disrupt insulin action.
Pentamidine, a drug prescribed to treat a
type of pneumonia, can increase the risk of
pancreatitis, beta cell damage, and diabetes.
Also, glucocorticoids—steroid hormones that
are chemically similar to naturally produced
cortisol—may impair insulin action. Glucocorticoids
are used to treat inflammatory illnesses
such as rheumatoid arthritis, asthma,
lupus, and ulcerative colitis.

Many chemical toxins can damage or destroy
beta cells in animals, but only a few have
been linked to diabetes in humans. For
example, dioxin—a contaminant of the herbicide
Agent Orange, used during the Vietnam
War—may be linked to the development of
type 2 diabetes. In 2000, based on a report
from the Institute of Medicine, the U.S.
Department of Veterans Affairs (VA) added
diabetes to the list of conditions for which
Vietnam veterans are eligible for disability
compensation. Also, a chemical in a rat poison
no longer in use has been shown to cause
diabetes if ingested. Some studies suggest a
high intake of nitrogen-containing chemicals
such as nitrates and nitrites might increase
the risk of diabetes. Arsenic has also been
studied for possible links to diabetes.

Lipodystrophy

Lipodystrophy is a condition in which fat tissue
is lost or redistributed in the body. The
condition is associated with insulin resistance
and type 2 diabetes.

Points to Remember

Diabetes is a complex group of diseases
with a variety of causes. Scientists
believe genes and environmental factors
interact to cause diabetes in most cases.

People with diabetes have high blood
glucose, also called high blood sugar or
hyperglycemia. Diabetes develops when
the body doesn’t make enough insulin
or is not able to use insulin effectively,
or both.

Insulin is a hormone made by beta cells
in the pancreas. Insulin helps cells
throughout the body absorb and use
glucose for energy. If the body does not
produce enough insulin or cannot use
insulin effectively, glucose builds up in
the blood instead of being absorbed by
cells in the body, and the body is starved
of energy.

Prediabetes is a condition in which
blood glucose levels or A1C levels are
higher than normal but not high enough
to be diagnosed as diabetes. People
with prediabetes can substantially
reduce their risk of developing diabetes
by losing weight and increasing physical
activity.

The two main types of diabetes are
type 1 diabetes and type 2 diabetes.
Gestational diabetes is a third form
of diabetes that develops only during
pregnancy.

Type 1 diabetes is caused by a lack
of insulin due to the destruction of
insulin-producing beta cells. In type 1
diabetes—an autoimmune disease—the body’s immune system attacks and
destroys the beta cells.

Type 2 diabetes—the most common
form of diabetes—is caused by a combination
of factors, including insulin
resistance, a condition in which the
body’s muscle, fat, and liver cells do not
use insulin effectively. Type 2 diabetes
develops when the body can no longer
produce enough insulin to compensate
for the impaired ability to use insulin.

Scientists believe gestational diabetes
is caused by the hormonal changes
and metabolic demands of pregnancy
together with genetic and environmental
factors. Risk factors for gestational
diabetes include being overweight and
having a family history of diabetes.

Monogenic forms of diabetes are
relatively uncommon and are caused
by mutations in single genes that limit
insulin production, quality, or action in
the body.

Other types of diabetes are caused
by diseases and injuries that damage
the pancreas; certain chemical toxins
and medications; infections; and other
conditions.

Hope through Research

The National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK)
conducts and supports research into many
kinds of disorders, including diabetes.
Researchers throughout the United States
and the world are working to better understand,
prevent, and treat this disease. Finding
ways to prevent or delay diabetes in
people at risk is a key goal of this research.
Scientists are identifying genes that may be
involved in type 1 or type 2 diabetes and
studying how they work. Studies are clarifying
the complicated mechanisms that damage
beta cells in diabetes. A great deal of work
is also focused on preventing the different
types of diabetes and improving treatment.

The NIDDK conducts research in its own
laboratories and supports a great deal of
basic and clinical research in medical centers
and hospitals throughout the United States.
Several other components of the NIH also
conduct and support research related to
diabetes. Other Government agencies that
sponsor diabetes programs are the Centers
for Disease Control and Prevention, the
Indian Health Service, the Health Resources
and Services Administration, the VA, and the
U.S. Department of Defense. In addition,
many organizations outside the Government
support diabetes research and education
activities. These organizations include the
ADA, the Juvenile Diabetes Research Foundation
International, the American Association
of Diabetes Educators, the American
Association of Clinical Endocrinologists, and
The Endocrine Society.

Clinical trials are research studies involving people. Clinical trials look at safe and effective new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. To learn more about clinical trials, why they matter, and how to participate, visit the NIH Clinical Research Trials and You website at www.nih.gov/health/clinicaltrials. For information about current studies, visit www.ClinicalTrials.gov.

Acknowledgments

Publications produced by the Clearinghouse
are carefully reviewed by both NIDDK
scientists and outside experts. This publication
was reviewed by Alan Shuldiner, M.D.,
University of Maryland.

You may also find additional information about this topic by visiting MedlinePlus at www.medlineplus.gov.

This publication may contain information about medications and, when taken as prescribed, the conditions they treat. When prepared, this publication included the most current information available. For updates or for questions about any medications, contact the U.S. Food and Drug Administration toll-free at 1–888–INFO–FDA (1–888–463–6332) or visit www.fda.gov. Consult your health care provider for more information.

National Diabetes Education
Program

The National Diabetes Education Program is
a federally funded program sponsored by the
U.S. Department of Health and Human Services’
National Institutes of Health and the
Centers for Disease Control and Prevention
and includes over 200 partners at the federal,
state, and local levels, working together to
reduce the morbidity and mortality associated
with diabetes.

National Diabetes Information Clearinghouse

The National Diabetes Information Clearinghouse (NDIC) is a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The NIDDK is part of the National Institutes of Health of the U.S. Department of Health and Human Services. Established in 1978, the Clearinghouse provides information about diabetes to people with diabetes and to their families, health care professionals, and the public. The NDIC answers inquiries, develops and distributes publications, and works closely with professional and patient organizations and Government agencies to coordinate resources about diabetes.

This publication is not copyrighted. The Clearinghouse encourages users of this publication to duplicate and distribute as many copies as desired.